Lung cancer is the most leading cause of
cancer-related death worldwide, with
non-small-cell lung cancer (NSCLC) accounting for over 80% of all
lung cancer cases. Patients with NSCLC are mostly treated with
platinum-based
chemotherapy. Chemoresistance is a leading cause of chemo-
therapy failure in NSCLC treatment. Recent studies have shown that dysregulation of
microRNAs might modulate the resistance of
cancer cells to anti-
cancer drugs, yet the modulation mechanism is not fully understood. In this paper, we try to test whether miR-192 regulates chemo-resistance in human
carcinoma A549 mice model by targeting Bcl-2. Mice model of human
lung adenocarcinoma was built up, and was used for
gemcitabine and
cisplatin combined
chemotherapy. MTT assay, real-time RT-PCR, western blotting assay were used to investigate miR-192 expression levels, cell viability ratio and Bcl-2
protein expression levels. MiR-192 expression level in A549 cells is significantly higher than in normal human bronchial epithelial cells. MiR-192 inhibitor treated
tumor exhibits sensitivity to
cisplatin and
gemcitabine therapy. Bcl-2
mRNA and
protein expression levels up-regulated in miR-192 inhibitor treated
tumor. Bcl-2 is a key regulator for miR-192 related
chemotherapy resistance. In this study, we demonstrate that miR-192 regulates chemoresistance for
gemcitabine and
cisplatin combined
chemotherapy in human
adenocarcinoma lung cancer A549 cells, and Bcl-2 is the target of miR-192.